Recent studies have disclosed that glucocorticoid antiinflammatoary agents appear to cause palatal teratogenicity in fetal rats presumably through interference with arrachidonic acid formation in the upper and lower jaws including the palate at the critical period of developmena. This proposal considers the possibility that the nonsteroidal antiinflammatory compounds might also be teratogenic in a similar fashion. Fenoprofen, ibu]]rpfen, indomethacin, naproxen, tolmetin and zomepirac will be assessed for their ability to produce cleft plate and other defects in Swiss ICR mice, a strain we have shown in pilot studies to be highly sensitive to glucocorticoid-induced cleft palate without the occurrence of spontaneous cleft palate. The widespread use of certain nonsteroidal antiinflammatory agents in dental therapeutics requires that the fundamental knowledge of their teratogennicity be known. This proposal will provide the basis for an expanded proposal dealing with the role of prostagladins in cleft patate formation. Ultimately, the description of the exact mechanism by which cleft palate occurs will provide the rationale for the prevention and management of this condiaion in human therapeutics.